Abstract

Behavioral traits associated with various forms of psychopathology are conceptualized as dimensional, varying from those present in a frank disorder to subclinical expression. Demonstrating links between these behavioral traits and neurobiological indicators, such as brain structure, provides one form of validation for this view. However, unlike behavioral dimensions associated with other forms of psychopathology (e.g., autism spectrum disorder, attention deficit hyperactivity disorder, antisocial disorders), eating disorder traits have not been investigated in this manner in spite of the potential that such an approach has to elucidate etiological mechanisms. Therefore, we examined for the first time neural endophenotypes of Anorexia Nervosa and Bulimia via dimensional traits (measured using the Eating Disorders Inventory-3) in a large subclinical sample of young adults (n = 456 and n = 247, respectively; ages = 18–22 years) who each provided a structural magnetic resonance imaging scan. Cortical thickness was quantified at 81,924 vertices across the cortical surface. We found: 1) increasing eating disorder traits correlated with thinner cortex in the insula and orbitofrontal cortex, among other regions, and 2) using these regions as seeds, increasing eating disorder trait scores negatively modulated structural covariance between these seed regions and other cortical regions linked to regulatory and sensorimotor functions (e.g., frontal and temporal cortices). These findings parallel those found in the clinical literature (i.e., thinner cortex in these food-related regions in individuals with eating disorders) and therefore provide evidence supporting the dimensional view of behavioral traits associated with eating disorders. Extending this approach to genetic and neuroimaging genetics studies holds promise to inform etiology.

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Acknowledgements

We thank all members of the Laboratory of NeuroGenetics for their assistance in conducting the Duke Neurogenetics Study, which was supported by Duke University and NIH grant R01DA033369. A.R.H. is further supported by NIH grant R01AG049789. We also thank Esha Mehta and Caylynn Yao for their assistance in completing this research.

Funding

This study was supported by Duke University and NIH grant R01DA033369. A.R.H. is further supported by NIH grant R01AG049789.

Compliance with ethical standards

Conflict of interest

The authors have no conflicts of interest relevant to this article to disclose.

Ethical approval

This study was approved by the Duke University Institutional Review Board.

Informed consent

All participants provided informed consent.

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